The working hypothesis is that reversible physical, functional and ultrastructural changes in surfactant occur in various conditions associated with alveolar collapse and a change in pattern of ventilation. Three rat models will be used: mechanical ventilation without sighs, exposure to toxic oxygen levels, and unilateral pulmonary artery ligation. The techniques used will include: (1) biochemical: phospholipid determinations, sedimentation; (2) physiological: volume measurements, pressure volume relationships, frequency and volume of tidal volumes and sighs; (3) surface chemistry: area-surface tension curves, adsorption properties; (4) ultrastructural: quantitation of the tubular myelin form of surfactant in sedimented pellets from lung lavage and in the in situ fixed alveolar lining layer. The significance is that alterations in the pattern of ventilation may cause physicochemical and ultrastructural changes in surfactant to a functionally less active form (tubular myelin) leading to increased alveolar surface tension, alveolar atelectasis, and predisposing to pulmonary edema.